Hi, real world, again!

The Mammal has emerged from a thesis-induced supermassive black hole and a Christmas-induced food coma, only to find that in the month or so that she spent barely functional and buried in chapters covered in the supervisor’s dreaded Red Pen, things actually happened in the world outside. This, naturally, manifested in thousands of items feeling thoroughly neglected in RSS readers and email inboxes. (Jesus. How many times have I vowed never to neglect my RSS feed again? Oh well, it’s not like unemployment is such a busy occupation that I can’t deal with a measly two and a half thousand articles 😛 )

… earlier tonight, the paragraph here said I wasn’t doing a proper post yet, “just pointing out” a couple of the cooler things I’ve missed. Then somehow this thing morphed into a 1000+ word post that goes way beyond “pointing things out”. It’s almost like I’ve been itching to write something that isn’t my thesis. >_>

So the first cool thing I wanted to “point out” is the genome paper of the centipede Strigamia maritima, which is a rather nondescript little beast hiding under rocks on the coasts of Northwest Europe. This is the first sequenced genome of a myriapod – the last great class of arthropods to remain untouched by the genome sequencing craze after many genomes from insects, crustaceans and chelicerates (spiders, mites and co.).  The genome sequence itself has been available for years (yay!), but its “official” paper (Chipman et al., 2014) is just recently out.

Part of the appeal of Strigamia – and myriapods in general – is that they are considered evolutionarily conservative for an arthropod. In some respects, the genome analysis confirms this. Compared to its inferred common ancestor with us, Strigamia has lost fewer genes than insects, for example. Quite a lot of its genes are also linked together similarly to their equivalents in distantly related animals, indicating relatively little rearrangement in the last 600 million years or so. But this otherwise conservative genome also has at least one really unique feature.

Specifically, this centipede – which is blind – has not only lost every bit of DNA coding for known light-sensing proteins, but also all known genes specific to the circadian clock. In other animals, genes like clock and period mutually regulate one another in a way that makes the abundance of each gene product oscillate in a regular manner (this is about the simplest graphical representation I could find…). The clock runs on a roughly daily cycle all by itself, but it’s also connected to external light via the aforementioned light-sensing proteins, so we can constantly adjust our internal rhythms according to real day-night cycles.

There are many blind animals, and many that live underground or otherwise find day and night kind of irrelevant, but even these are often found to have a functioning circadian clock or keep some photoreceptor genes around. However, based on the genome data, our favourite centipede may be the first to have completely lost both. The authors of the genome paper hypothesise that this may be related to the length of evolutionary time the animals have spent without light. Things like mole rats are relatively recent “inventions”. However, the geophilomorph order of centipedes, to which Strigamia belongs, is quite old (its most likely sister group is known from the Carboniferous, so they’re probably at least that ancient). Living geophilomorphs are all blind, so chances are they’ve been that way for the last 300+ million years.

Nonetheless, the authors also note that geophilomorphs are still known to avoid light – the question now is how the hell they do it… And, of course, whether Strigamia has a clock is not known – only that it doesn’t have the clock we’re used to. We also have no idea at this point how old the gene losses actually are, since all the authors know is that one other centipede from a different group has perfectly good clock genes and opsins.

In comparison with fruit flies and other insects, the Strigamia genome also reveals some of the ways in which evolutionary cats can be skinned in multiple ways. There is an immune-related gene family we share with arthropods and other animals, called Dscam. The product of this gene is involved in pathogen recognition among other things, and in flies, Dscam genes are divided into roughly 100 chunks or exons, most of which are are found in clusters of variant copies. When the gene is transcribed, only one of these copies is used from each such cluster, so in practical terms the handful of fruit fly Dscam genes can encode tens of thousands of different proteins, enough to adapt to a lot of different pathogens.

A similar arrangement is seen in the closely related crustaceans, although with fewer potential alternative products. In other groups – the paper uses vertebrates, echinoderms, nematodes and molluscs for comparison – the Dscam family is pretty boring with at most one or two members and none of these duplicated exons and alternative splicing business. However, it looks like insects+crustaceans are not the only arthropods to come up with a lot of DSCAM proteins. Strigamia might also make lots of different ones (“only” hundreds in this case), but it achieved this by having dozens of copies of the whole gene instead of performing crazy editing feats on a small number of genes. Convergent evolution FTW!

Before I paraphrase the entire paper in my squeeful enthusiasm (no, seriously, I’ve not even mentioned the Hox genes, and the convergent evolution of chemoreceptors, and I think it’s best if I shut up now), let’s get to something else that I can’t not “point out” at length: a shiny new vetulicolian, and they say it’s related to sea squirts!

Vetulicolians really deserve a proper discussion, but in lieu of a spare week to read up on their messiness, for now, it’s enough to say that these early Cambrian animals have baffled palaeontologists since day one. Reconstructions of various types look like… a balloon with a fin? Inflated grubs without faces? I don’t know. Drawings below (Stanton F. Fink, Wikipedia) show an assortment of the beasts, plus Yunnanozoon, which may or may not have something to do with them. Here are some photos of their fossils, in case you wondered.

Vetulicolians from Wiki

They’re certainly difficult creatures to make sense of. Since their discovery, they’ve been called both arthropods and chordates, and you can’t get much farther than that with bilaterian animals (they’re kind of like the Nectocaris of old, come to think of it…).

The latest one was dug up from the Emu Bay Shale of Australia, the same place that yielded our first good look at anomalocaridid eyes. Its newest treasure has been named Nesonektris aldridgei by its taxonomic parents (García-Bellido et al., 2014), and it looks something like this (Diego García-Bellido’s reconstruction from the paper):


In other words, pretty typical vetulicolian “life but not as we know it”, at first glance. Its main interest lies in the bit labelled “nc” in the specimens shown below (from the same figure):


This chunky structure in the animal’s… tail or whatever is a notochord, the authors contend. Now, only one kind of animal has a notochord: a chordate. (Suspicious annelid muscle bundles notwithstanding. Oh yeah, I also wanted to post on Lauri et al. 2014. Oops?) So if this thing in the middle of Nesonektris’s tail is a notochord, then at the very least it is more closely related to chordates than anything else.

Why do they think it is one? Well, there are several long paragraphs devoted to just that, so here goes a summary:

1. It’s probably not the gut. A gut would be the other obvious ID, but it doesn’t fit very well in this case. Structures interpreted as guts in other vetulicolians – which sometimes contain stuff that may be half-digested food – (a) start in the front half of the body, where the mouth is, (b) constrict and expand and coil and generally look much floppier than this, (c) don’t look segmented, (d) sometimes occur alongside these tail rod-like thingies, so probably aren’t the same structure.

2. It positively resembles modern half-decayed notochords. The notochords of living chordates are long stacks of (muscular or fluid-filled) discs, which fall apart into big blocks as the animal decomposes after death. Here’s what remains of the notochord of a lamprey after two months for comparison (from Sansom et al. (2013)):


This one isn’t as regular as the blockiness in the fossils, I think, but that could just be the vetulicolians not being quite as rotten.

There is, of course, a but(t). To be precise, there are also long paragraphs discussing why the structure might not be a notochord after all. It’s much thicker than anything currently interpreted as such in reasonably clear Cambrian chordates, for one thing. Moreover, it ends right where the animal does, in a little notch that looks like a good old-fashioned arsehole. By the way, the paper notes, vetulicolian tails in general don’t go beyond their anuses by any reasonable interpretation of the anus, and a tail behind the anus is kind of a defining feature of chordates, though this study cites a book from the 1970s claiming that sea squirt larvae have a vestigial bit of proto-gut going all the way to the tip of the tail. (I suspect that claim could use the application of some modern cell labelling techniques, but I’ve not actually seen the book…)

… and there is a phylogenetic analysis, in which, if you interpret vetulicolians as deuterostomes (which impacts how you score their various features), they come out specifically as squirt relatives whether or not you count the notochord. I’m never sure how much stock to put in a phylogenetic analysis based on a few bits of anatomy gleaned from highly contentious fossils, but at least we can say that there are other things – like a hefty cuticle – beyond that notochord-or-not linking vetulicolians to a specific group of chordates.

Having reached the end, I don’t feel like this paper solved anything. Nice fossils either way 🙂

And with that, I’m off. Maybe next time I’ll write something that manages to be about the same thing throughout. I’ve been thinking that I should try to do more posts about broader topics rather than one or two papers (like the ones I wrote about ocean acidification or homology versus developmental genetics), but I’ve yet to see whether I’ll have the willpower to handle the necessary reading. I’m remarkably lazy for someone who wants to know everything 😀

(Aside: holy crap, did I ALSO miss a fucking Nature paper about calcisponges’ honest to god ParaHox genes? Oh my god, oh my GOD!!! *sigh* This is also a piece of incredibly exciting information I’ve known for years, and I miss it when it actually comes out in a journal bloody everyone reads. You can tell I’ve been off-planet!)


Chipman AD et al. (2014) The first myriapod genome sequence reveals conservative arthropod gene content and genome organisation in the centipede Strigamia maritima. PLoS Biology 12:e1002005

García-Bellido DC et al. (2014) A new vetulicolian from Australia and its bearing on the chordate affinities of an enigmatic Cambrian group. BMC Evolutionary Biology 14:214

Lauri A et al. (2014) Development of the annelid axochord: insights into notochord evolution. Science 345:1365-1368

Sansom RS et al. (2013) Atlas of vertebrate decay: a visual and taphonomic guide to fossil interpretation. Palaeontology 56:457-474

Only so many ways

In a way, the limitations of evolution are more interesting to me than its possibilities. It’s cool to figure out how exquisite adaptations and fantastically complex molecular machines might have evolved, but I like my evolution the way Brandon Sanderson likes his magic. If it can do anything, then where’s the fun? Deep underlying rules and constraints are what make it really interesting.

Convergent evolution can hint at such rules. Some of them are just physics and seem pretty straightforward. If you’re a creature swimming in the sea, being streamlined is good for you, and there aren’t that many ways of being streamlined. So dolphins, squid and sharks have the same basic shape despite coming from very different ancestors. Other cases involve more subtle and probably more interesting constraints. The baggage of your ancestry, the interactions in your genome, the pool of available mutations, can all restrict the ways in which you can adapt to a particular challenge. A study I found in the huge backlog of random pdfs on my desktop probes tentatively into the importance of such intrinsic limitations.

Conte et al. (2012) asked a seemingly simple question that has apparently never been systematically investigated before: how often does convergent or parallel evolution of the same trait result from modification of the same genes?

Convergent and parallel evolution are sort of two ends of a continuum. We use parallel evolution to refer to traits that evolved in similar directions starting from the same starting point. For example, three-spine sticklebacks repeatedly lost their bony armour when they moved from the sea to rivers and lakes in various places around the world. The ancestor is the same heavily armoured marine fish in each case, and most freshwater populations underwent very similar changes (including their genetic basis) from this common beginning. At the other end of the scale you find clear instances of convergence, such as “milk” in mammals and birds. Their common ancestors not only didn’t ooze custom-made immune-boosting baby food, they likely didn’t even care for their young.

Back to the paper. Conte et al. conducted what we call a meta-analysis: collecting and analysing data from all published studies that fit their pre-determined set of criteria. Altogether, they looked at a carefully selected set of 25 studies about the genetic basis of convergent traits. Not too great, the authors acknowledge, but it’s a start.

The studies were divided into two sets, because the two main methods of looking at the genetic basis of a trait can’t easily be analysed together. The first set contained genetic mapping studies (“which parts of the genome cause X?”), and the second candidate gene studies (“does this gene cause X?”). The convergent traits in these studies were quite diverse. There was pale skin from cave fish to humans, African and European peoples’ ability to digest lactose as adults, resistance to tetrodotoxin in snakes, wing patterns in butterflies, electric organs in fish…

The comparisons span quite a long time scale. On one end, there are populations within a single species, like lactose-tolerant Europeans and Arabs, that diverged mere tens of thousands of years ago. On the other, pale-skinned cave fish and Swedes are separated by something on the order of 400 million years. This is part of what makes this an exciting study, because you can indirectly observe what happens to genetic constraints over time.

The most exciting, though, is the sheer amount of gene re-use the researchers saw. For mapping studies, they found a 32% chance that the same trait will be associated with the same gene(s) in different species. Candidate genes give an even higher estimate (55%), but that might just be the nature of the beast. When a candidate gene is not behaving as expected it’s probably less interesting and publishable, Conte et al. argue, whereas mapping studies will usually throw up something to write about.*

Within a species, the probability of the same gene being used in the same adaptation gets as high as 80% for both methods. This is despite the fact that often the traits in question are controlled by several genes, any of which could be mutated to the same effect. Where you come from clearly has a huge impact on where (and how) you can go. The impact lessens as you look at increasingly distant species; at a hundred million years of divergence, mapping data show only 10% similarity between convergent traits, and even candidate genes drop to around 40%. (Methinks 10% is still a big number considering how many genes we have, but of course we’re talking about relatively simple traits here, so the number of relevant genes isn’t nearly as high.)

There are some logical possible explanations behind both the high level of genetic convergence in close relatives and the big drop with increasing divergence. For example, it could be that populations within a species have very similar pools of genetic variation. If the same genes vary, then natural selection will “naturally” hit on the same genes when adaptation becomes handy. It’s also likely that the rest of the genome plays a part – closely related populations/species have more similar genetic backgrounds, their genes likely interact with one another in more similar ways, ergo the restrictions on what mutations can become beneficial are also similar. As lineages diverge, so do such interactions and restrictions, lowering the probability that two species evolve the same trait in the same way.

Of course, it’s at this point impossible to say which of the potential reasons actually cause the trends observed in this study, but that wasn’t the point. The authors’ stated goals were pretty modest:

“[O]ur aim here has been to stimulate thinking about these issues and to move towards a quantitative understanding of repeated genetic evolution” (p5044)

In that, I hope, they have succeeded. It’d be lovely to see more of this “big picture” discussion of convergent evolution. Big pictures make Mammals happy.


*I’m not sure about that, myself. I think if you’ve got a gene that’s been shown to do X in species after species, a negative finding is a lot more newsworthy than yet another confirmation of the same old shit. I suppose it’s gut feeling versus intuition until someone does a study of that, though 🙂



Conte GL et al. (2012) The probability of genetic parallelism and convergence in natural populations. Proceedings of the Royal Society B 279:5039-5047

Animals, amoebae and plant scientists’ concerns

I recently wondered, in response to an “ideas” paper in BioEssays, whether animals, fungi, slime moulds etc. actually had a multicellular common ancestor. Dickinson and colleagues’ argument (partly) hinged on the shared presence of epithelia, “barrier” cell layers with distinct insides and outsides, in animals and the social amoeba Dictyostelium discoideum. The most recent crop from BioEssays includes a short letter by František Baluška of the botany department at the University of Bonn that challenges this argument.

Plants, Baluška reminds us, also have epithelia. These epithelia are functionally more similar to animals’ than the one Dickinson’s team found in the amoebae. While there may be doubts about amoebae, plants almost certainly became multicellular independently of animals. Ergo, convergent evolution can clearly produce similar tissues in two distant lineages. So why would we take the possession of an epithelium as evidence for a multicellular common ancestor?

Which is a perfectly valid argument, but it misses the point in my opinion.

The botanist writes,

[Plants] evolved their own plant-specific epithelia 3–5, obviously via convergent evolution. This fact alone not only continues to make plausible the traditional independent origin of multicellularity in the metazoa and social amoebae, but it also indicates that the power of convergent evolution should not be underestimated.

Of course it shouldn’t, but Dickinson’s team wasn’t arguing that “the traditional independent origin of multicelluarity” in animals and amoebae was not plausible any more. They find it unlikely that the functional and molecular similarity (does the latter exist between plants and animals?) between animal and amoeba epithelia is convergent, but they are suggesting that we investigate their new hypothesis, not that we summarily throw out the old one. Baluška is attacking a straw man.

Furthermore, he only addresses this one argument, but the thing in the Dickinson article that made me think the most was phylogeny. According to the traditional scenario, it seemed more likely that all those different unikont groups evolved multicellularity independently. But multicellularity is very widespread among unikonts, so precisely what makes the traditional scenario more likely? (Incidentally, has anyone done any actual statistics on this?)

As far as I’m concerned, the letter said nothing to change my mind. Dickinson et al. presented an interesting idea that’s definitely worth a closer look. I don’t think the evidence is currently strong enough to upset the consensus, but the proposal is not at all daft. I have to say I agree that plants should not be ignored, though. Because we can assume that any similarity between them and animals when it comes to being multicellular is the result of convergence, they’d be a wonderful “control group” when people start testing Dickinson et al.‘s hypothesis.

I think that’s something students of evolution should always keep in mind. Plants and animals have little reason to do things in the same way – they diverged very long ago, adapted to completely different lifestyles, etc. If they do so anyway, that might tell us something deeper about the way living things work. A limitation imposed by physics, a very ancient genetic predisposition, or simply the best way to do something – either way, finding the reason will enrich our knowledge of life and evolution. Animal scientists would be well advised to remember that.



Baluška F (2012) Rethinking origins of multicellularity: Convergent evolution of epithelia in plants. BioEssays, available online 26/10/2012, doi: 10.1002/bies.201200134

So… much… STUFF!

Gods, this is what I’m faced with all the time. Someone needs to tell me how proper science bloggers pick articles to discuss, because I just get my RSS alerts, start squeeing, and end up not writing about anything because damn, I WANT TO WRITE ABOUT EVERYTHING!

I give up. I’ll just dump all the cool stuff that’s accumulated on my desktop and bookmark bar here and return to lengthy meandering whenever I don’t feel like I’ve been caught in a bloody tornado 😉

So, here is some Cool Stuff…

(1) A group measured the rate of DNA decay in 158 moa bones of known age from three sites. Really cool stuff, to go out and directly measure how ancient DNA disappears from dead things under more or less identical conditions. The unsurprising result is that DNA decays exponentially, a bit like radioactive material. This suggests that the main cause of the decay is random breaking of the strands. The surprising bit is that this happens much more slowly than previously estimated, suggesting that in ideal (read: frozen) conditions, it might be worth looking for preserved DNA in samples as old as a million years.

(On a side note, if you ever get a chance to see a talk by Eske Willerslev, one of the authors and a leading expert on ancient DNA, don’t miss it. The man is absolutely hilarious.)

– Allentoft ME et al. (2012) The half-life of DNA in bone: measuring decay kinetics in 158 dated fossils. Proceedings of the Royal Society B FirstCite article, available online 10/10/2012, doi: 10.1098/rspb.2012.1745

(2) The beaks of the finches, or mixing and matching developmental recipes. This study examines the genetic basis of beak shape in three little birds closely related to Darwin’s famous finches. The three finches, just like Darwin’s, share the same basic beak shape, only bigger or smaller. However, there seem to be two distinct developmental programs at work, using different genes and parts of the skeleton to orchestrate beak development. One of the three newly investigated species (the one most closely related to Darwin’s finches) apparently uses the same developmental program as its more famous relatives, even though its beak is shaped more like the other two birds studied here. I told you – genetics, development and homology are complicated 😉

– Mallarino R et al. (2012) Closely related bird species demonstrate flexibility between beak morphology and underlying developmental programs. PNAS 109:16222–16227

(3) Armoured fossil links worm-like molluscs to chitons. There’s a little-known group (or groups) of molluscs called aplacophorans that have only a coat of tiny spicules instead of shells and look more like worms than “proper” molluscs. Exactly where they fit into our picture of mollusc evolution has been controversial to say the least – they could represent an old lineage separate from other molluscs, they could be related to cephalopods, they could be related to chitons, they could be one group or they could be two lineages in completely different places on the tree… Well, a new fossil named Kulindroplax seems to argue for the chiton connection: the animal has the characteristic armour plates of a chiton on an aplacophoran-like body. Similar creatures have been discovered before, but this guy with its detailed 3D preservation provides the clearest evidence of the link so far.

– Sutton MD et al. (2012) A Silurian armoured aplacophoran and implications for molluscan phylogeny. Nature 490:94-97

(4) More cool fossils – this time straight from my beloved Cambrian. Nereocaris, a newly described Burgess Shale arthropod, suggests to its discoverers that the earliest arthropods weren’t predators prowling the seafloor, but swimmers who might have been filter feeders and certainly weren’t predators. The animal has a bivalved shell around its front end, similar to many other Cambrian swimming arthropods, and a long abdomen with paddles at the end. It bears the arthropod hallmark of a hardened and jointed exoskeleton, but it lacks specialised limbs such as antennae or mouthparts. In a cladistic analysis of arthropods and their nearest relatives, the new species comes out on the first branch within true arthropods, and the next few branches as we move towards living arthropods all contain similar shelled, swimming creatures. Since the non-arthropods closest to the real thing (i.e. anomalocaridids) were also fin-tailed swimmers, this arrangement makes the transition between them and true arthropods smoother than previously thought. It also suggests that the hard exoskeleton so characteristic of arthropods originally functioned in swimming – perhaps as an anchor for swimming muscles.

– Legg DA et al. (2012) Cambrian bivalved arthropod reveals origin of arthrodization. Proceedings of the Royal Society B FirstCite article, available online 10/10/2012, doi: 10.1098/rspb.2012.1958


And … there was also

… but it’s almost bedtime, and if I wanted to summarise every one of those, I’d be here all weekend 😦

See, this is why being a science nerd today is both amazing and frustrating. There’s just so. Much. Stuff.

A virus with half a wing

Richard Lenski’s team is one of my favourite research groups in the whole world. If the long-term evolution experiment with E. coli was the only thing they ever did, they would already have earned my everlasting admiration. But they do other fascinating evolution stuff as well. In their brand new study in Science (Meyer et al., 2012), they explore the evolution of a novelty – in real time, at single nucleotide resolution.

For their experiments, they used a pair of old enemies: the common gut bacterium and standard lab microbe E. coli, and one of its viruses, the lambda phage. Phages (or bacteriophages, literally “bacterium eaters”) are viruses that infect bacteria. They are also some of mother nature’s funkiest-looking children. Below is an example, because if you haven’t seen one of them, you really should. I borrowed this electron micrograph of phage T4 from GiantMicrobes, where you can get a cute plushie version 😛

Phages work by latching onto specific proteins in the cell membrane of the bacterium, and literally injecting their DNA into the cell, where it can start wreaking havoc and making more viruses. Meyer et al.‘s phage strain was specialised to use an E. coli protein called LamB for attachment.

The team took E. coli which (mostly) couldn’t produce LamB because one of the lamB gene’s regulators had been knocked out. Their virus normally couldn’t infect these bacteria, but a few of the bacteria managed to switch lamB on anyway, so the viruses could vegetate along in their cultures at low numbers. Perfect setup for adaptation!

Meyer and colleagues performed a lot of experiments, and I don’t want to go into too much detail about them (hey, is that me trying not to be verbose???). Here are some of their intriguing results:

First, the phages adapted to their LamB-deficient hosts. They did so very “quickly” in terms of what we usually think of as evolutionary time scales (naturally, “evolutionary time scales” mean something different for organisms with life cycles measurable in minutes). Mutations in the gene coding for their J protein (the one they use to attach to LamB) enabled them to use another bacterial protein instead. Not all experimental populations evolved this ability, but those that did succeeded in less than 2 weeks on average.

The new protein target, OmpF, is quite similar to LamB, which might explain how the viruses evolved the ability to use it so quickly. But more interesting than the speed is the how of their innovation. Amazingly, all OmpF-compatible viruses shared two specific mutations. Another mutation always occurred in the same codon, that is, it affected the same amino acid in the J protein. A fourth mutation invariably occurred in a short region near the other three. Altogether, these four mutations allowed the virus to use OmpF. Plainly, we are dealing with more than mere convergent evolution here. Often, many different mutations can achieve the same thing (see e.g. Eizirik et al., 2003), but in this case, a very specific set of them appeared necessary. I’ll briefly revisit this point later, but first we have another fascinating result to discuss!

By comparing dozens of viruses that did and didn’t evolve OmpF compatibility, the researchers determined that all four mutations were necessary for the new ability. Three were not enough; there were many viral strains with three of the four mutations that couldn’t do anything with LamB-deficient bacteria. On the surface, this sounds almost like something Michael Behe would say (see Behe and Snokes, 2004), except the requirement for more than one mutation clearly didn’t prevent innovation here. Given the distribution of J mutations, it’s also likely that they were shaped by natural selection, even in virus populations that didn’t evolve OmpF-compatibility. So what did the first three mutations do? What use was, as it were, half a new J protein?

The answer would delight the late Stephen Jay Gould: the new function was a blatant example of exaptation. Exaptations are traits that originally had one function, but were later co-opted for another. While three mutations predisposed the J gene to OmpF-compatibility, they also improved its ability to bind its original target. Thus, there was a selective advantage right from the first mutation. And, in essence, this is what we see over and over again when we look at novelties. Fish walk underwater, non-flying dinosaurs cover their eggs with feathered arms, and none of them have the first clue that their properties would become success stories for completely different reasons.

In the paper, there is a bit of discussion on co-evolution and how certain mutations in the bacteria influenced the viruses’ ability to adapt to OmpF, but I’d like to go back to the convergence/necessity point instead. I have a few half-formed thoughts here, so don’t expect me to be coherent 😉

We’ve seen cases where the same outcome stems from different causes, like in the cat colour paper cited above. Then there is this new function in a virus that seems to always come from (almost) the same set of mutations. Why? I’m thinking it has to do with (1) the complexity of the system, (2) the type of outcome needed.

Proteins interact with other proteins through very specific interfaces. Sometimes, these interactions can depend on as little as a single amino acid in one of the partners. If you want to change something like that, there is simply little choice in what you can do without screwing everything up. On the other hand, something like coat colour in mammals is controlled by a whole battery of genes, each of which may be amenable to many useful modifications. And when it comes to even more complex traits like flying (qv. aside discussing convergence and vertebrate flight/gliding in the mutations post), the possibilities are almost limitless.

So there’s that, and there is also what you “want” with a trait. There may be more ways to break a gene (e.g. to lose pigmentation) than to increase its activity. When the selectively advantageous outcome is something as specific as a particular protein-protein interaction, the options may be more restricted again. (To top that, the virus has to stick to the bacterium with a very specific part in its structure, or the whole “inject DNA” bit goes the wrong way.) Now that I read what I wrote that sounds like there will be very few “universal laws” of evolutionary novelty (exaptation being one of them?). Hmm…


Behe MJ and Snoke DW (2004) Simulating evolution by gene duplication of protein features that require multiple amino acid residues. Protein Science 13:2651-2664

Eizirik E et al. (2003) Molecular genetics and evolution of melanism in the cat family. Current Biology 13:448-453

Meyer JR et al. (2012) Repeatability and contingency in the evolution of a key innovation in phage lambda. Science 335:428-432